ArticleJournal of neuroinflammation2019
Mesenchymal stem cells alleviate the early brain injury of subarachnoid hemorrhage partly by suppression of Notch1-dependent neuroinflammation: involvement of Botch.
Article in Journal of neuroinflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 4 of them syntheses that pooled it.
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Who cites it
56 citing papers in PubMed, 4 syntheses or guidelines pooled it, 112 citations in OpenAlex.
- A Systematic Review of Inflammatory Cytokine Changes Following Aneurysmal Subarachnoid Hemorrhage in Animal Models and Humans.Translational stroke research · 2022Pooled it
- Gene Polymorphisms Increasing the Risk of Intracranial Aneurysms: Interleukin-1β -511C>T (Part I).Acta bio-medica : Atenei Parmensis · 2022Pooled it
- Gene Polymorphisms Increasing the Risk of Intracranial Aneurysms: Interleukin-6 -174G>C and -572G>C (Part II).Acta bio-medica : Atenei Parmensis · 2022Pooled it
- Mesenchymal stem cells-derived therapies for subarachnoid hemorrhage in preclinical rodent models: a meta-analysis.Stem cell research & therapy · 2022Pooled it
- Machine Learning-Based Integration Unveils RNA Methylation Regulator-Related Immune-Derived Gene Signatures in Ruptured Intracranial Aneurysm.Biomedicines · 2026Article
- Early Detection of Cerebral Vasospasm Following Aneurysmal Subarachnoid Hemorrhage by IL-6 Electrochemiluminescence Analysis of the Cerebrospinal Fluid.Diagnostics (Basel, Switzerland) · 2026Article
- Mesenchymal stem cells and secretome as modulators of neuroinflammation in neurological disorders.Journal of translational medicine · 2026Review
- Clinical Applications of Extracellular Vesicles: Promises and Pitfalls.International journal of molecular sciences · 2026Review
- Mesenchymal stem cells in treating human diseases: molecular mechanisms and clinical studies.Signal transduction and targeted therapy · 2025Review
- Article
- Olfactory mucosa mesenchymal stem cell-derived exosomes protect against neuroinflammation after subarachnoid hemorrhage by activating mitophagy.The Kaohsiung journal of medical sciences · 2025Article
- Astrocyte-microglia crosstalk in subarachnoid hemorrhage: mechanisms and treatments.Frontiers in immunology · 2025Review
- Progress of bone marrow mesenchymal stem cell transplantation on neural plasticity in brain.Frontiers in cell and developmental biology · 2025Review
- The strategic breakdown: CHAC enzymes as regulators of glutathione homeostasis and disease implications.Frontiers in molecular biosciences · 2025Review
- The sentinel against brain injury post-subarachnoid hemorrhage: efferocytosis of erythrocytes by leptomeningeal lymphatic endothelial cells.Theranostics · 2025Article
- Downregulation of Notch Signaling-Stimulated Genes in Neurovascular Unit Alterations Induced by Chronic Cerebral Hypoperfusion.Immunity, inflammation and disease · 2024Article
- Hepcidin depending on astrocytic NEO1 ameliorates blood-brain barrier dysfunction after subarachnoid hemorrhage.Cell death & disease · 2024Article
- Review
- Ferroptosis in early brain injury after subarachnoid hemorrhage: review of literature.Chinese neurosurgical journal · 2024Review
- Mesenchymal stem cell-derived exosomes regulate microglia phenotypes: a promising treatment for acute central nervous system injury.Neural regeneration research · 2023Review
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
backgroundActivated microglia-mediated neuroinflammation has been regarded as an underlying key player in the pathogenesis of subarachnoid hemorrhage (SAH)-induced early brain injury (EBI). The therapeutic potential of bone marrow mesenchymal stem cells (BMSCs) transplantation has been demonstrated in several brain injury models and is thought to involve modulation of the inflammatory response. The present study investigated the salutary effects of BMSCs on EBI after SAH and the potential mechanism mediated by Notch1 signaling pathway inhibition.
methodsThe Sprague-Dawley rats SAH model was induced by endovascular perforation method. BMSCs (3 × 10
resultsBMSCs treatment mitigated the neurobehavioral dysfunction, BWC and BBB disruption associated with EBI after SAH, reduced ionized calcium binding adapter molecule 1 and cluster of differentiation 68 staining and interleukin (IL)-1 beta, IL-6 and tumor necrosis factor alpha expression in the left hemisphere but concurrently increased IL-10 expression. DAPT or Notch1 siRNA administration reduced Notch1 signaling pathway activation following SAH, ameliorated neurobehavioral impairments, and BBB disruption; increased BWC and neuronal degeneration; and inhibited activation of microglia and production of pro-inflammatory factors. The augmentation of Notch1 signal pathway agents and phosphorylation of nuclear factor-κB after SAH were suppressed by BMSCs but the levels of Botch were upregulated in the ipsilateral hemisphere. Botch knockdown in BMSCs abrogated the protective effects of BMSCs treatment on EBI and the suppressive effects of BMSCs on Notch1 expression.
conclusionsBMSCs treatment alleviated neurobehavioral impairments and the inflammatory response in EBI after SAH; these effects may be attributed to Botch upregulation in brain tissue, which subsequently inhibited the Notch1 signaling pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.